Recombinant Human Hepatocyte growth factor receptor (MET), partial

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Code CSB-EP013714HU1
Size US$306
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  • (Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel.

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Product Details

Greater than 85% as determined by SDS-PAGE.
Target Names
Uniprot No.
Research Area
Epigenetics and Nuclear Signaling
Alternative Names
AUTS9; c met; D249; Hepatocyte growth factor receptor; HGF; HGF receptor; HGF/SF receptor; HGFR; MET; Met proto oncogene; Met proto oncogene tyrosine kinase; MET proto oncogene; receptor tyrosine kinase; Met proto-oncogene (hepatocyte growth factor receptor); Met proto-oncogene; Met protooncogene; MET_HUMAN; Oncogene MET; Par4; Proto-oncogene c-Met; RCCP2; Scatter factor receptor; SF receptor; Tyrosine-protein kinase Met
Homo sapiens (Human)
Expression Region
Target Protein Sequence
Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
Mol. Weight
59.4 kDa
Protein Length
Tag Info
C-terminal 6xHis-tagged
Liquid or Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
If the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol.
Note: If you have any special requirement for the glycerol content, please remark when you place the order.
If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. Our default final concentration of glycerol is 50%. Customers could use it as reference.
Troubleshooting and FAQs
Storage Condition
Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life
The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time
3-7 business days
Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet & COA
Please contact us to get it.

The synthesis of Recombinant Human MET protein began with the isolation of MET gene from the native genome. The next step was to amplify the MET gene by inserting the MET gene into an expression vector and then introducing the vector into the selected host cell, E.coli. Significant amounts of recombinant Human MET protein were produced by the host only when expression genes were added. For the purpose of protein purification, the vector contains C-terminal 6xHis tag to the MET DNA sequence. The purity of this protein is 85%+ determined by SDS-PAGE.

MET, also known as the N-methyl-N’-nitroso-guanidine human osteosarcoma transforming gene, is a proto-oncogene encoding a receptor tyrosine kinase c-MET for hepatocyte growth factor (HGF). The binding of HGF results in c-MET dimerization and autophosphorylation, which in turn activates the mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase (PI3K), v-src avian sarcoma (Schmidt-Ruppin A-2) viral oncogene homolog (SRC), and signal transducer and activator of transcription (STAT) signaling pathways. The MET pathway plays an important role in wound healing, post-injury response, and degenerative diseases such as renal and lung fibrosis. Aberrant MET expression is widely observed in various malignancies, particularly non-small cell lung cancer (NSCLC), gastrointestinal (GI) cancer, and hepatocellular carcinoma (HCC). MET-receptor overexpression, genomic amplification, mutation, or alternative splicing results in cellular deregulation of MET.

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Target Background

Receptor tyrosine kinase that transduces signals from the extracellular matrix into the cytoplasm by binding to hepatocyte growth factor/HGF ligand. Regulates many physiological processes including proliferation, scattering, morphogenesis and survival. Ligand binding at the cell surface induces autophosphorylation of MET on its intracellular domain that provides docking sites for downstream signaling molecules. Following activation by ligand, interacts with the PI3-kinase subunit PIK3R1, PLCG1, SRC, GRB2, STAT3 or the adapter GAB1. Recruitment of these downstream effectors by MET leads to the activation of several signaling cascades including the RAS-ERK, PI3 kinase-AKT, or PLCgamma-PKC. The RAS-ERK activation is associated with the morphogenetic effects while PI3K/AKT coordinates prosurvival effects. During embryonic development, MET signaling plays a role in gastrulation, development and migration of muscles and neuronal precursors, angiogenesis and kidney formation. In adults, participates in wound healing as well as organ regeneration and tissue remodeling. Promotes also differentiation and proliferation of hematopoietic cells. May regulate cortical bone osteogenesis.; (Microbial infection) Acts as a receptor for Listeria monocytogenes internalin InlB, mediating entry of the pathogen into cells.
Gene References into Functions
  1. the miR-19a/c-Met pathway plays a critical role in acquired resistance to gefitinib and that the manipulation of miR-19a might provide a therapeutic strategy for overcoming acquired gefitinib resistance. PMID: 28592790
  2. The expression of C-Met and HER2 protein in lung adenocarcinoma is highly correlated, and whether it is synergistic in the targeted therapy of lung adenocarcinoma deserves further study. PMID: 29400000
  3. MET overexpression was more frequently found in high grade myxofibrosarcoma and the epithelioid variant. Chromosome 7 polysomy, rather than MET gene regional amplification, might account for the overexpression. of MET protein. PMID: 30126419
  4. miR-449a suppresses hepatocellular carcinoma tumorigenesis by down-regulating activity in the c-Met/ERK pathway. PMID: 30108016
  5. We found MET amplifications in two cases of endometrial clear-cell carcinoma with mixed features. PMID: 29633423
  6. Regarding gene mutation abundance, NGS enables the detection of low-abundant ctDNA in blood based on ultra-deep sequencing, and our patient benefited from crizotinib despite the low abundance of MET exon 14 skipping. These data indicate that we can choose targeted therapy despite the low abundance of gene mutations. PMID: 29110851
  7. The interplay of dual MET/HER2 overexpression in the AKT and ERK pathways for esophageal cancer is described. Therefore, combination therapy could be a novel strategy for EAC with amplification of both MET and HER2. PMID: 29223420
  8. MET inactivation in the context of the BRAF-activating mutation is driven through a negative feedback loop involving inactivation of PP2A phosphatase, which in turn leads to phosphorylation on MET inhibitory Ser985. PMID: 30224486
  9. MET Exon 14 Skipping Mutations in Non-small Cell Lung Cancer PMID: 30037377
  10. MET activation, by either METex14 mutations or amplification, is characteristic of a subset of early stage NSCLCs and may coexist with ERBB2 amplification. PMID: 29139039
  11. Results demonstrate that serum level of miR-658 is significantly lower in the NM group than in the DM group. Meanwhile, the levels of PAX3 and MET are lower in the NM group than in the DM group too. Both overexpression and silence of miR-658 significantly up-regulate or down-regulate the levels of PAX3 and MET in gastric cell lines. PMID: 29630524
  12. MiR-206 inhibits the development of epithelial ovarian cancer cell by directly targeting c-Met and inhibiting the c-Met/AKT/mTOR signaling pathway. PMID: 29807226
  13. These results suggest that gastric cancer progression is not associated with a unique signaling pathway and that a feedback loop may exist between the HGF/c-Met and Notch1 signaling pathways, which may result in therapeutic resistance. PMID: 29781036
  14. Comparative analysis revealed a strong association between MET expression and MET amplification (85% concurrence) in primary stomach tumors and matched liver metastasis. Survival analyses revealed that both MET amplification and MET overexpression were prognostic of poor outcomes. PMID: 29790169
  15. High c-met expression is associated with oral squamous cell carcinoma. PMID: 29286169
  16. FOXO1 serves as an important linker between HER2 and MET signaling pathways through negative crosstalks and is a key regulator of the acquired lapatinib resistance in HER2-positive GC cells. PMID: 28343375
  17. analysis of how the cMET blockade augments radiation therapy in patients with NF2 PMID: 29440379
  18. these findings highlight the relevance of cross-species protein interactions between murine feeder cells and human epithelial cells in 3T3-J2 co-culture and demonstrate that STAT6 phosphorylation occurs in response to MET activation in epithelial cells. However, STAT6 nuclear translocation does not occur in response to HGF, precluding the transcriptional activity of STAT6. PMID: 29771943
  19. c-Met-activated Mesenchymal Stem Cells (MSC) pre-exposed to hypoxia interact with PrPC at the site of ischemic injury to increase the efficiency of MSC transplantation. PMID: 29705776
  20. A novel G-quadruplex motif formed in the Human MET promoter region. PMID: 29054971
  21. a METex14 del mutation-positive NSCLC patient who responded to crizotinib but later relapsed, demonstrated a mixed response to glesatinib including reduction in size of a MET Y1230H mutation-positive liver metastasis and concurrent loss of detection of this mutation in plasma DNA. Together, these data demonstrate that glesatinib exhibits a distinct mechanism of target inhibition and can overcome resistance to PMID: 28765324
  22. This study demonstrates that simultaneous inhibition of c-Met and Src signaling in MD-MSCs triggers apoptosis and reveals vulnerable pathways that could be exploited to develop NF2 therapies. PMID: 28775147
  23. prolonged treatment of single HGF/c-Met or Hh inhibitor leads to resistance to these single inhibitors, likely because the single c-Met treatment leads to enhanced expression of Shh, and vice versa. Targeting both the HGF/c-Met and Hh pathways simultaneously overcame the resistance to the single-inhibitor treatment and led to a more potent antitumor effect in combination with the chemotherapy treatment. PMID: 28864680
  24. We identified unique and tumor-specific tyrosine phosphorylation rewiring in tumors resistant to treatment with the irreversible third-generation EGFR-inhibitor, osimertinib, or the novel dual-targeting EGFR/Met antibody, JNJ-61186372. PMID: 28830985
  25. TGF-beta negatively controls the HGF/c-MET pathway by regulating of stemness in glioblastoma. PMID: 29238047
  26. The preclinical efficacy and safety data provide a clear rationale for the ongoing clinical studies of Sym015 in patients with MET-amplified tumors. PMID: 28679766
  27. High MET expression is associated with malignant pleural mesothelioma. PMID: 28560410
  28. the results of real-time PCR and western blotting revealed that Huaier extract decreased p65 and c-Met expression and increased IkappaBalpha expression, while paclitaxel increased p65 expression and reduced IkappaBalpha and c-Met expression.The molecular mechanisms may be involved in the inhibition of the NF-kappaB pathway and c-Met expression PMID: 29039556
  29. Data found that the expression of c-Met was significantly increased in human oral squamous cell carcinoma (OSCC) tissues than in normal mucosa adjacent to the tumor, but was not correlated with clinicopathological parameters. Also, further findings indicated the potential role of c-Met in the progression of OSCC. PMID: 29115556
  30. Our data show that S49076 exerts its cytotoxic activity at low doses on MET-dependent cells through MET inhibition, whereas it inhibits growth of MET-independent cells at higher but clinically relevant doses by targeting Aurora B PMID: 28619752
  31. MET expression was shown to be significantly reduced in the superior temporal gyrus cortex of autism spectrum disorders individuals. PMID: 28322981
  32. In SCCHN, immunohistochemical overexpression of c-MET above cut-off levels III and particularly II was associated with inferior survival outcomes and advanced disease PMID: 29103754
  33. Here we present a case series of three such patients who achieved were cMET amplified and showed partial response on Crizotinib PMID: 29199685
  34. c-Met/beta1 integrin complex whose ligand-independent cross-activation and robust affinity for fibronectin drives invasive oncologic processes. PMID: 28973887
  35. tivantinib did not suppress MET signaling, and selective MET inhibitors demonstrated an antiproliferative effect only in MHCC97H, the unique cell line displaying MET gene amplification. HCC tumors with high expression of cell proliferation genes defined a group of patients with poor survival. PMID: 28246274
  36. Studies show that MET mutations have been found in cancer of unknown primary origin (CUP) being clustered to the SEMA and TK domain of the receptor. The biomechanical properties of MET mutants might trigger the hyper-invasive phenotype associated to CUP. [review] PMID: 29037604
  37. Data show that Kruppel like factor 4 (KLF4) was overexpressed in met proto-oncogene protein (c-Met)-overexpressing non-small-cell lung cancer (NSCLC) cells and tissues. PMID: 29624806
  38. SOCS1 attenuates migration and invasion properties of hepatocellular carcinoma cells at least partly via modulation of MET-mediated epithelial-mesenchymal transition, and controls invasive tumor growth. PMID: 29085209
  39. The authors reconfirmed EGFR mutation as a strong predictive marker of Non-Small-Cell Lung Cancer. However, c-MET positivity was not associated with response or progression-free survival, although c-MET overexpression correlated with some clinical characteristics. PMID: 29502124
  40. findings show oncogene E5 is primarily responsible for Met upregulation; E5-induced Met contributes motility of HPV-containing cells; these studies show a new role for E5 in epithelial-stromal interactions, with implications for cancer development PMID: 29609071
  41. EGFR T790M mutation and cMET amplification are main mechanisms leading to EGFR TKI resistance in lung adenocarcinoma. PMID: 29616327
  42. MET activation is associated with drug resistance in chronic myeloid leukemia. PMID: 28418880
  43. High glucose activated Met receptor in HK2 cells independently of HGF, via induction of integrin a5b1 and downstream signaling. This mode of Met activation was associated with tubular cell damage and apoptosis and it may represent a novel pathogenic mechanism and a treatment target in diabetic nephropathy. PMID: 28819999
  44. The purpose of this study was to explore gene copy number (GCN) variation of EGFR, HER2, c-MYC, and MET in patients with primary colorectal cancer. PMID: 28764718
  45. HGF/c-MET pathway mediates VEGFR inhibitor resistance and vascular remodeling in NSCLC. PMID: 28559461
  46. Because c-Met is strongly associated with pathological grade, stage and disease-specific survival, c-Met levels may have potential to predict patient prognosis and to guide clinical diagnosis and treatment of patients with renal cell carcinoma PMID: 28427859
  47. miR-1 is downregulated in ovarian cancer tissues, and may play a tumor suppressive role by inhibiting c-Met expression and its effects on the regulation of cell proliferation, migration and invasion PMID: 28698064
  48. Proto-oncogene proteins c-met (MET) mutations Y1248H and D1246N confer resistance in vitro and in vivo. PMID: 28396313
  49. MET overexpression is found in 23.8% of surgically resected NSCLC. MET amplification prevails in 4.6% and is associated with MET overexpression. Both have no influence on prognosis. PMID: 28838386
  50. study highlights the role of tissue differentiation on pathological response to neoadjuvant chemotherapy in gastric cancer and shows no impact between FOXP3, HER2 and MET expression in terms of tumor regression grading PMID: 29696715

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Involvement in disease
Hepatocellular carcinoma (HCC); Renal cell carcinoma papillary (RCCP); Deafness, autosomal recessive, 97 (DFNB97); Osteofibrous dysplasia (OSFD)
Subcellular Location
Membrane; Single-pass type I membrane protein.; [Isoform 3]: Secreted.
Protein Families
Protein kinase superfamily, Tyr protein kinase family
Tissue Specificity
Expressed in normal hepatocytes as well as in epithelial cells lining the stomach, the small and the large intestine. Found also in basal keratinocytes of esophagus and skin. High levels are found in liver, gastrointestinal tract, thyroid and kidney. Also
Database Links

HGNC: 7029

OMIM: 114550

KEGG: hsa:4233

STRING: 9606.ENSP00000317272

UniGene: Hs.132966

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